31 results on '"Makbule Aydin"'
Search Results
2. DNA Repair Gene Variants in Migraine
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Makbule Aydin, Elif Ozkok, Yılmaz Çetinkaya, Elif Sinem Bireller, Selcuk Dasdemir, Bedia Cakmakoglu, and Mehmet Gencer
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Adult ,Male ,DNA Repair ,DNA repair ,Migraine Disorders ,Population ,Disease ,Biology ,Bioinformatics ,DNA Glycosylases ,Pathogenesis ,XRCC3 ,Cricetinae ,DNA-(Apurinic or Apyrimidinic Site) Lyase ,medicine ,Animals ,Humans ,education ,Genotyping ,Genetics (clinical) ,Xeroderma Pigmentosum Group D Protein ,Genetics ,education.field_of_study ,Polymorphism, Genetic ,General Medicine ,Middle Aged ,medicine.disease ,DNA-Binding Proteins ,Migraine ,Etiology ,Female - Abstract
Migraine is a common and debilitating episodic disorder characterized by recurrent headache attacks associated with autonomic symptoms. It affects an estimated 12% of the population. The etiology of the underlying neurodegenerative process is widely unknown; however, oxidative stress is a unifying factor in the current theories of migraine pathogenesis. After demonstrating the observation that oxidative DNA damage is detectable in migraine disease, searching the role played by DNA repair systems in migraine diseases could bring us much significant information about the pathogenesis of migraine. We prospectively investigated whether DNA repair gene polymorphisms (XRCC1 Arg399Gln, XRCC3 Thr241Met XPD Lys751Gln, XPG Asp1104His, APE1 Asp148Glu, hOGG1 Ser326Cys) account for an increased risk of migraine. The present analyses are based on 135 case subjects with migraine disease and 101 noncase subjects. Genotyping of DNA repair gene polymorphisms (XRCC1 Arg399Gln, XRCC3 Thr241Met XPD Lys751Gln, XPG Asp1104His, APE1 Asp148Glu, hOGG1 Ser326Cys) was detected by polymerase chain reaction-restriction fragment length polymorphism.We demonstrated that apurinic endonuclease (APE), X-ray repair complementing defective repair in Chinese hamster cells 3 (XRCC3), xeroderma pigmentosum D (XPD), and hOGG1 gene variants were associated with an increased risk for development of migraine disease (p0.05). In contrast, no statistically significant differences were found in genotype distributions of X-ray repair complementing defective repair in Chinese hamster cells 1 (XRCC1) and XPG between migraine cases and controls (p0.05).Our findings have suggested that APE1, XRCC3, XPD, and hOGG1 gene variants could facilitate the development of migraine disease.
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- 2014
3. Cox-2 gene variants in migraine
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Yılmaz Çetinkaya, Selcuk Dasdemir, Bedia Cakmakoglu, Elif Ozkok, Mehmet Gencer, and Makbule Aydin
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Adult ,Male ,Oncology ,medicine.medical_specialty ,Adolescent ,Genotype ,Migraine Disorders ,Disease ,Osteoarthritis ,Pharmacology ,Biology ,Polymerase Chain Reaction ,Polymorphism, Single Nucleotide ,Pathogenesis ,Young Adult ,Gene Frequency ,Polymorphism (computer science) ,Internal medicine ,Genetics ,medicine ,Humans ,Genetic Predisposition to Disease ,Genotyping ,Genetic Association Studies ,General Medicine ,Middle Aged ,medicine.disease ,Haplotypes ,Migraine ,Cyclooxygenase 2 ,Rheumatoid arthritis ,Female ,Polymorphism, Restriction Fragment Length - Abstract
Migraine is a multifactorial and complex disorder, and any clear diagnostic marker to assess the status of the migraineurs has not been established, yet. Nonsteroidal anti-inflammatory drugs reduce production of prostanoids including PGE2 by inhibiting COX-1 and/or COX-2, and thereby suppress inflammatory pain in patients suffering from rheumatoid arthritis, osteoarthritis, and migraine. Thus, COX-2 regulation is important in the pathogenesis and treatment of migraine. We prospectively investigated COX-2-765G→C and COX-2-1195A→G gene polymorphisms which may account for an increased risk of migraine.The present analyses are based on 144 case subjects with migraine disease and 123 non-case subjects. Genotyping of COX-2 gene polymorphisms (COX-2-765G→C, COX-2-1195A→G) was detected by PCR-RFLP.We, for the first time, demonstrated positive association of COX-2 gene variants with an increased risk for development of migraine. Carriers of COX-2-765 C+ genotype in controls were higher than in the patients (57.7% and 36.1% respectively; P0.0001) and the frequencies of G+ genotype in patients were higher than in the controls (97.9% and 88.6% respectively; P: 0.002). In addition, frequencies of COX-2-765 GG and GC genotypes in patients were higher than in the controls (P0.0001, P0.0001 respectively). It seems that COX-2-765 G+ genotype had increased and COX-2-765 C+ genotype had decreased risk for migraine. In COX-2-1195 polymorphism only AG genotype was statistically significantly different in patients than in the controls (P0.05).Our findings have suggested that COX-2-765 G+ genotype could facilitate the development of migraine disease.
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- 2013
4. DNA Repair Genes in Parkinson's Disease
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Elif Ozkok, Yılmaz Çetinkaya, Hülya Tireli, Mehmet Gencer, Selcuk Dasdemir, Figen Varlibas, Cem İsmail Küçükali, Bedia Cakmakoglu, and Makbule Aydin
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Male ,DNA Repair ,Genotype ,DNA repair ,DNA damage ,Polymerase Chain Reaction ,Polymorphism, Single Nucleotide ,XRCC1 ,Gene Frequency ,XRCC3 ,Risk Factors ,DNA-(Apurinic or Apyrimidinic Site) Lyase ,Humans ,Genetic Predisposition to Disease ,Genotyping ,Allele frequency ,Genetics (clinical) ,Polymerase ,Aged ,Genetics ,biology ,Parkinson Disease ,General Medicine ,Middle Aged ,DNA-Binding Proteins ,X-ray Repair Cross Complementing Protein 1 ,biology.protein ,Female ,Polymorphism, Restriction Fragment Length - Abstract
There is a growing interest in the understanding of a possible role of DNA repair systems in ageing and neurodegenerative diseases after DNA damage is observed in the brain of individuals affected by neurodegenerative diseases. In the light of these findings, we investigated whether DNA repair gene polymorphisms (XRCC1 Arg399Gln, XRCC3 Thr241Met XPD Lys751Gln, XPG Asp1104His, APE1 Asp148Glu, and HOGG1 Ser326Cys) account for an increased risk of Parkinson's disease (PD).The present analyses are based on 60 case subjects with PD and 108 unrelated healthy controls. Genotyping of DNA repair gene polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism.We, for the first time, demonstrated the positive association of APE1, XRCC1, and XRCC3 DNA repair gene variants with PD risk. In our study, the frequencies of Glu/Glu genotype in APE1, Gln+ genotype of XRCC1, and Thr+ genotype of XRCC3 are higher in patients than in controls (p=0.028, p=0.002 and p=0.046, respectively).In conclusion, our findings have suggested that APE1, XRCC1, and XRCC3 genetic variants may be a risk factor by increasing oxidative stress that might cause the loss of dopaminergic cells in the substantiata nigra and locus caeruleus, leading to abnormal signal transmittion, and ultimately, the development of PD. In addition, generation of reactive oxygen species from dopamine might affect the other DNA repair pathway proteins that we did not examine in the current study. Further studies with larger sample groups are necessary to clarify the role of DNA repair genes and the development of PD.
- Published
- 2012
5. Increased risk of advanced prostate cancer associated with MnSOD Ala-9-Val gene polymorphism
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Canan Kucukgergin, Makbule Aydin, Oner Sanli, Faruk Özcan, Sule Seckin, and Tzevat Tefik
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Male ,medicine.medical_specialty ,Genotype ,Disease ,Biology ,Polymerase Chain Reaction ,Gastroenterology ,Statistics, Nonparametric ,Prostate cancer ,Surveys and Questionnaires ,Internal medicine ,Odds Ratio ,Genetics ,medicine ,Humans ,Genetic Predisposition to Disease ,Molecular Biology ,Genetic Association Studies ,Aged ,DNA Primers ,Polymorphism, Genetic ,medicine.diagnostic_test ,Superoxide Dismutase ,Smoking ,Age Factors ,Prostatic Neoplasms ,General Medicine ,Rectal examination ,Odds ratio ,Middle Aged ,Prostate-Specific Antigen ,medicine.disease ,Manganese Superoxide Dismutase ,Increased risk ,Immunology ,Gene polymorphism ,Polymorphism, Restriction Fragment Length - Abstract
We aimed to investigate the association between manganese superoxide dismutase (MnSOD) Ala-9-Val gene polymorphism and the initiation and/or progression of prostate cancer (PCa) as well as to evaluate its potential interactions with advanced age and smoking status. MnSOD Ala-9-Val gene polymorphism was carried out in 134 (mean age 64.1 ± 7.48) PCa patients and 159 (mean age 62.5 ± 7.53) healthy controls with serum prostate specific antigen (PSA) levels (
- Published
- 2011
6. Homocysteine and pro-inflammatory cytokine concentrations in acute heart disease
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Yesim Unlucerci, Elif Ozkok, Cahide Gokkusu, Makbule Aydin, Feti Tulubas, and Berrin Umman
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medicine.medical_specialty ,Acute coronary syndrome ,Hyperhomocysteinemia ,Homocysteine ,medicine.medical_treatment ,Immunology ,Inflammation ,Disease ,Biochemistry ,chemistry.chemical_compound ,Folic Acid ,Internal medicine ,Humans ,Immunology and Allergy ,Medicine ,Risk factor ,Interleukin 6 ,Molecular Biology ,Demography ,biology ,Interleukin-6 ,business.industry ,Hematology ,Middle Aged ,medicine.disease ,Vitamin B 12 ,Cytokine ,Endocrinology ,ROC Curve ,chemistry ,Cardiovascular Diseases ,Case-Control Studies ,biology.protein ,Interleukin-2 ,medicine.symptom ,business - Abstract
Inflammation is involved in development and progression of atherosclerosis. Interleukin-2 (IL-2) and interleukin-6 (IL-6) have been correlated with various cardiovascular diseases. Hyperhomocysteinemia is an important risk factor for atherosclerosis and thrombotic disease. Recent studies have demonstrated that homocysteine (Hcy) enhances productions of several pro-inflammatory cytokines. In the light of these findings, we decided to determine if any relationship exists between IL-2 and IL-6, the pro-inflammatory cytokines, and total homocysteine (tHcy) in acute coronary syndrome (ACS). A total of 102 patients with ACS and 90 healthy subjects were included in the study. The levels of tHcy, IL-2 and IL-6 were higher and folic acid was lower in patients as compared with those of controls. Furthermore, data of the area under ROC plot for IL-2 demonstrated that IL-2 had higher sensitivity. These data suggest that enhanced inflammation may be associated with tHcy-related cardiovascular disease.
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- 2010
7. Do schizophrenia and bipolar disorders share a common disease susceptibility variant at the MMP3 gene?
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Elif Ozkok, Cem İsmail Küçükali, Makbule Aydin, Ihsan Kara, Emine Bilge, Asli Zengin, and Nurcan Orhan
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Adult ,Male ,medicine.medical_specialty ,Psychosis ,Bipolar Disorder ,Bipolar I disorder ,Genetic Linkage ,DNA Mutational Analysis ,Biology ,Polymorphism, Single Nucleotide ,Gene Frequency ,Genetic linkage ,Molecular genetics ,Genotype ,medicine ,Humans ,Genetic Predisposition to Disease ,Bipolar disorder ,Allele ,Biological Psychiatry ,Psychiatric Status Rating Scales ,Pharmacology ,Genetics ,Chi-Square Distribution ,Middle Aged ,medicine.disease ,body regions ,Genetic epidemiology ,Schizophrenia ,Female ,Matrix Metalloproteinase 3 - Abstract
There is growing evidence of partial etiological overlap between schizophrenia (SZ) and bipolar I disorder (BD-I) from linkage analysis, genetic epidemiology and molecular genetics studies. SZ and BD-I are neurodevelopmental disorders with genetic and environmental etiologies. Recent studies have demonstrated that matrix metalloproteinase 3 (MMP3) is a key event in associative memory formation, learning and synaptic plasticity, which are important in psychiatric disorders. In the light of these findings, we analyzed the genetic variations in the MMP3-1171 5A/6A in patients with SZ, patients with BD-I and healthy controls. To the best of our knowledge, this is the first study to report an association of variation in gene encoding MMP3 with SZ. Our study group consisted of 111 unrelated patients with SZ, 141 unrelated patients with BD-I, and 121 unrelated healthy controls. The frequencies of 6A6A genotype and 6A allele distributions of MMP3 in patients with SZ were significantly decreased when compared with controls. In contrast, in patients with SZ, the distributions of 5A5A genotype and 5A allele of MMP3 gene were significantly increased as compared with healthy controls. When the frequencies of genotypes or alleles in schizophrenic patients and bipolar patients were compared, 6A6A genotype and 6A allele in patients with BD-I were significantly higher than patients with SZ. In contrast, 5A5A genotype and 5A allele distributions of MMP3 gene were significantly frequent in patients with SZ. On the other hand, no significant differences were found in the allele or genotype distribution in patients with BD-I compared with controls. In conclusion, our data have supported the hypothesis that there is a possible relationship between − 1171 5A/6A polymorphism of MMP3 gene and SZ. A larger sample group is needed to confirm the potential role of this gene in the pathophysiology of psychiatric disorders.
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- 2009
8. Paraoxonase-1 55/192 genotypes in schizophrenic patients and their relatives in Turkish population
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Ulku Cakir, Cem İsmail Küçükali, Gamze Kilic, Makbule Aydin, Ihsan Kara, Elif Ozkok, Nurhan Ince, Zeynep Ozbek, and Nurcan Orhan
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Adult ,Male ,medicine.medical_specialty ,Turkish population ,Genotype ,Turkey ,behavioral disciplines and activities ,Internal medicine ,mental disorders ,Genetics ,Humans ,Medicine ,Genetic Predisposition to Disease ,In patient ,Biological Psychiatry ,Genetics (clinical) ,biology ,Aryldialkylphosphatase ,business.industry ,Paraoxonase ,Middle Aged ,medicine.disease ,PON1 ,Pathophysiology ,Psychiatry and Mental health ,Schizophrenia ,Case-Control Studies ,Toxicity ,biology.protein ,Female ,business - Abstract
Oxidative stress and free radical-induced toxicity have been implicated in the pathophysiology of schizophrenia. In this study, we examined paraoxonase (PON1)-55/192 polymorphisms and PON1 activity in patients with schizophrenia, first-degree relatives of schizophrenic patients, and healthy controls.This study consisted of 292 healthy participants, 267 unrelated patients with schizophrenia and 311 first-degree relatives of schizophrenic patients. PON1 55 (rs 854560) and PON1 192 (rs 662) polymorphisms were performed by restriction fragment length polymorphism.The frequencies of the QQ and LL genotypes were significantly overpresented in controls compared with those of schizophrenic patients and their relatives. In contrast, the RR genotype was more prevalent in patients than their relatives and healthy controls. The frequencies of the LM and QR genotypes in relatives were higher than controls. Serum PON1 activities of controls were significantly higher when compared with both schizophrenic patients and their relatives. The RR and LL genotypes were associated with a significantly increased PON1 activity as compared with QR or QQ and MM or LM genotypes, respectively, in all groups.This is the first study that shows the association between PON1-55/192 polymorphisms and schizophrenia. Our data suggest that the subjects carrying R allele or RR genotype might be susceptible to schizophrenia and subjects with QQ or LL might be protected against schizophrenia. First-degree relatives of schizophrenic patients have higher heterozygote genotypes, suggesting that this group can shift either to patient or control group depending on their allele types and environmental factors. PON1 genetic variations are also associated with PON1 activities. Reduced PON1 activity in patients and their relatives might result from the combined effects of more than one polymorphic variant in PON1 or other genes and/or increased oxidative stress, supporting the hypothesis that reactive oxygen species-mediated cellular damage might contribute to the neuropathology of schizophrenia.
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- 2008
9. ACE Gene Polymorphism in Peripheral Vascular Disease
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Makbule Aydin, Murat Aksoy, Yılmaz Başar, Nihal Salmayenli, Elif Ozkok, and Sule Seckin
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Adult ,Male ,medicine.medical_specialty ,Ace gene polymorphism ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Peptidyl-Dipeptidase A ,Biology ,Biochemistry ,Endocrinology ,Gene Frequency ,Internal medicine ,Genotype ,medicine ,Humans ,In patient ,Peripheral Vascular Diseases ,chemistry.chemical_classification ,Polymorphism, Genetic ,Vascular disease ,Homozygote ,Biochemistry (medical) ,Angiotensin-converting enzyme ,General Medicine ,Middle Aged ,medicine.disease ,Peripheral ,Genotype frequency ,Enzyme ,chemistry ,Case-Control Studies ,biology.protein ,Female - Abstract
Peripheral vascular disease is an atherosclerotic process. It has been suggested that angiotensin converting enzyme insertion/deletion polymorphism is associated with atherosclerosis. The aim of this study was to investigate the role of the insertion/deletion polymorphism of the angiotensin-converting enzyme in Turkish patients with peripheral vascular disease in Western part of Turkey. We also investigated the relationship between serum angiotensin converting enzyme activity and distribution of genotypes in both patients and control group. The study group consisted of 78 patients with peripheral vascular disease. The control group consisted of 73 healthy adults. Serum angiotensin converting enzyme activities in patients were higher than those of the control group (p
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- 2007
10. Combined Effects of ACE and MMP-3 Polymorphisms On Migraine Development
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Yılmaz Çetinkaya, Hülya Tireli, Nurcan Orhan, Gamze Kilic, Elif Ozkok, Mehmet Gencer, Makbule Aydin, and Ihsan Kara
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Adult ,Male ,medicine.medical_specialty ,Adolescent ,Turkey ,Migraine Disorders ,Peptidyl-Dipeptidase A ,Matrix metalloproteinase ,Polymorphism, Single Nucleotide ,Risk Assessment ,law.invention ,Pathogenesis ,03 medical and health sciences ,0302 clinical medicine ,Risk Factors ,law ,Internal medicine ,Genotype ,Prevalence ,medicine ,Humans ,Genetic Predisposition to Disease ,030212 general & internal medicine ,Ace activity ,Allele ,Gene ,Polymerase chain reaction ,Aged ,business.industry ,General Medicine ,Middle Aged ,medicine.disease ,Endocrinology ,Migraine ,Disease Progression ,Female ,Matrix Metalloproteinase 3 ,Neurology (clinical) ,business ,030217 neurology & neurosurgery - Abstract
Migraine is a primary headache disorder which involves both genetic and environmental components. Since angiotensin-converting enzyme (ACE) and matrix metalloproteinase (MMP) share the same homology, we investigated whether the MMP-3 and ACE I/D gene variants are involved in migraine risk and whether the ACE variant might act in combination with the MMP-3 genetic variant in patients with migraine. This is the first study to evaluate the association between MMP-3 and ACE polymorphisms, and migraine. Genotypes were determined by polymerase chain reaction. The frequencies of 5A5A genotypes of the MMP-3 and D allele of ACE were significantly elevated, but II genotypes of the ACE and 6A allele of MMP-3 significantly decreased in all patients. The combined DD/5A5A and ID/5A5A genotypes increased the risk of migraine. Individuals who were homozygous for the deletion (D) allele showed increased ACE activity. Subjects with the 5A5A genotype and/or D allele or with the combined DD/5A5A or ID/5A5A might be more susceptible to migraine development. In contrast, subjects with the II and/or 6A6A genotypes may be protected from migraine development. The greater activity of the 5A5A and DD genotypes might result in vascular reactivity that is more pronounced in migraine. Taken together, our data suggest that numerous genes may influence ACE activity. Discovery of new genes might better clarify the pathogenesis of migraine and open an avenue to therapeutic strategies against migraine.
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- 2007
11. PON1 55/192 polymorphism, oxidative stress, type, prognosis and severity of stroke
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Makbule Aydin, Ihsan Kara, Cihat Örken, Mehmet Gencer, Yılmaz Çetinkaya, Gamze Kilic, Elif Ozkok, Zeynep Ozbek, and Hülya Tireli
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Male ,medicine.medical_specialty ,Glutamine ,Clinical Biochemistry ,Glutathione reductase ,Biology ,Arginine ,medicine.disease_cause ,Severity of Illness Index ,Biochemistry ,Gastroenterology ,chemistry.chemical_compound ,Methionine ,Leucine ,Risk Factors ,Polymorphism (computer science) ,Internal medicine ,Severity of illness ,Genetics ,medicine ,Humans ,Molecular Biology ,Allele frequency ,Stroke ,Aged ,Polymorphism, Genetic ,Aryldialkylphosphatase ,Cell Biology ,Prognosis ,Malondialdehyde ,medicine.disease ,PON1 ,Oxidative Stress ,Amino Acid Substitution ,chemistry ,Female ,Oxidative stress - Abstract
We investigated the association of PON1 55/192 polymorphisms with type, severity and prognosis of stroke and oxidative markers. Paraoxonase1 (PON1), Glutathione Reductase (GSH-Rd) and Malondialdehyde (MDA) levels were measured at day 1 and at day 5 following the onset of stroke. Genotypes were determined by polymerase chain reaction and restriction digestion. The frequencies of QQ and MM genotypes of PON1 192 and PON1 55, respectively, were significantly higher in controls than in patients. However, the allele frequencies of PON1 192 R and PON1 55 L were significantly more frequent in patients compared to controls. The frequency of combined genotype of RR/LL was significantly higher in cardioembolic group than in atherothrombotic group. PON1 activities were significantly diminished in stroke patients compared to controls. In contrast, serum MDA levels were significantly greater in patients than the values in controls. GSH-Rd activity was higher in patients with small lesion and good prognosis than those with large and poor prognosis. Low density lipoprotein (LDL) levels in patients with large lesions were higher than those with small lesions. PON1 55/192 polymorphisms influence activity of the enzyme. PON1 55/192 genotypes have been associated with MDA levels. In conclusion, PON1 genetic variations are associated with risk factors, severity, type and prognosis of stroke and oxidative stress.
- Published
- 2006
12. Identification of a novel BRCA2 and CHEK2 A-C-G-C haplotype in Turkish patients affected with breast cancer
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Fatmahan Atalar, Hazal Haytural, Gokce Akan, Elif Ozkok, Bedia Cakmakoglu, Nazlı Yalçınkaya, Makbule Aydin, Soykan Arikan, and Ilhan Yaylim
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Oncology ,Adult ,Cancer Research ,medicine.medical_specialty ,endocrine system diseases ,Genotype ,Turkey ,Epidemiology ,Population ,Breast Neoplasms ,Biology ,Breast cancer ,Risk Factors ,Internal medicine ,medicine ,Biomarkers, Tumor ,Humans ,Genetic Predisposition to Disease ,skin and connective tissue diseases ,education ,CHEK2 ,Aged ,Neoplasm Staging ,BRCA2 Protein ,education.field_of_study ,Haplotype ,Public Health, Environmental and Occupational Health ,Case-control study ,Middle Aged ,medicine.disease ,Prognosis ,Penetrance ,Genotype frequency ,Checkpoint Kinase 2 ,Haplotypes ,Case-Control Studies ,Mutation ,Cancer research ,Female ,Follow-Up Studies - Abstract
Background: Many breast cancers are caused by certain rare and familial mutations in the high or moderate penetrance genes BRCA1, BRCA2 and CHEK2. The aim of this study was to examine the allele and genotype frequencies of seven mutations in BRCA1, BRCA2 and CHEK2 genes in breast cancer patients and to investigate their isolated and combined associations with breast cancer risk. Methods: We genotyped seven mutations in BRCA1, BRCA2 and CHEK2 genes and then analyzed single variations and haplotype associations in 106 breast cancer patients and 80 healthy controls. Results: We found significant associations in the analyses of CHEK2- 1100delC (p=0.001) and BRCA1-5382insC (p=0.021) mutations in breast cancer patients compared to controls. The highest risk was observed among breast cancer patients carrying both CHEK2-1100delC and BRCA2- Met784Val mutations (OR=0.093; 95%CI 0.021-0.423; p=0.001). We identified one previously undescribed BRCA2 and a CHEK2 four-marker haplotype of A-C-G-C which was overrepresented (χ 2 =7.655; p=0.0057) in the patient group compared to controls. Conclusion: In this study, we identified a previously undescribed BRCA2 and CHEK2 A-C-G-C haplotype in association with the breast cancer in our population. Our results further suggest that the CHEK2-1100delC mutation in combination with BRCA2-Met784Val may lead to an unexpected high risk which needs to be confirmed in larger cohorts in order to better understand their role in the development and prognosis of breast cancer.
- Published
- 2013
13. Effect of Oxidative Stress on DNA Repairing Genes
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Bedia Cakmakoglu, Zeynep Birsu Cincin, and Makbule Aydin
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chemistry.chemical_classification ,DNA ligase ,biology ,Chemistry ,DNA polymerase ,DNA damage ,Base excision repair ,medicine.disease_cause ,AP endonuclease ,Biochemistry ,DNA glycosylase ,biology.protein ,medicine ,AP site ,Oxidative stress - Abstract
Oxidative DNA damage has been thought to contribute to the general decline in cellular functions that are associated with a variety of diseases including Alzheimer disease, amyotrophic lateral sclerosis (ALS), Parkinson’s disease, atherosclerosis, ischemia/reperfusion neuronal injuries, degenerative disease of the human temporomandibular-joint, cataract formation, macular degeneration, degenerative retinal damage, rheumatoid arthritis , multiple sclerosis , muscular dystrophy, diabetes mellitus, human cancers as well as the aging process itself. Oxidative stress occurs when the production of the reactive oxygen species (ROS) exceeds natural antioxidant defence mechanisms. There are several sources that form the ROS. Most of ROS come from the endogenous sources as by-products of normal and essential metabolic reactions, such as energy generation from mitochondria or the detoxification reactions involving the liver cytochrome P-450 enzyme system. There are also exogenous ROS sources including exposure to cigarette smoke, environmental pollutants such as emission from automobiles and industries, consumption of alcohol in excess, asbestos, exposure to ionizing radiation, and bacterial, fungal or viral infections. ROS cause damage to biomolecules such as lipid, proteins and DNA by attaching. ROS may directly attack DNA, either the sugar, phosphate or purine and pyrimidine bases. On the other hand, oxidative damage may be indirect by rising of intracellular Ca+2 ions. Free radical-mediated reactions can cause structural alterations in DNA (e.g., nicking, base-pair mutations, rearrangement, deletions insertions and sequence amplification). Degradation of the bases will produce numerous products, including 8-OH-Gua, hydroxymethylurea, urea, thymine glycol; thymine and adenine ring opened and saturated products. Most oxidized bases in DNA are repaired by base excision repair (BER). BER consists of four main steps. The first step involves the removal of the oxidised base by a specific DNA glycosylase, yielding an apurinic/apyrimidinic (AP) site. In the second step, an AP endonuclease removes the deoxyribose phosphate group from the AP site generating a single nucleotide gap. A DNA polymerase, thought to be predominantly DNA polymerase b, fills this gap. Finally, a DNA ligase, probably DNA ligase III, seals the stand break and completes the repair process. This chapter mainly deals with: (i) formation of ROS in physiological and pathological conditions, (ii ) ROS-mediated DNA damage, leading to cellular pathology and ultimately to cell death (iii) Oxidative DNA damage repair systems, (iv) The molecular mechanism of ROS-mediated diseases such as cancer, cardiovascular disease, neurodegenerative diseases, inflammatory disease, ischemia-reperfusion injury and aging.
- Published
- 2011
14. Genetic variants in nuclear-encoded mitochondrial proteins are associated with oxidative stress in obsessive compulsive disorders
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Makbule Aydin, Ulku Cakir, Nurcan Orhan, Cem İsmail Küçükali, and Nildan Seker
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Adult ,Male ,medicine.medical_specialty ,Pathology ,Obsessive-Compulsive Disorder ,Antioxidant ,Genotype ,Mitochondrial disease ,medicine.medical_treatment ,Biology ,medicine.disease_cause ,Polymorphism, Single Nucleotide ,Ion Channels ,Linkage Disequilibrium ,Mitochondrial Proteins ,chemistry.chemical_compound ,Polymorphism (computer science) ,Internal medicine ,Malondialdehyde ,medicine ,Odds Ratio ,Humans ,Uncoupling Protein 2 ,Allele ,Biological Psychiatry ,Retrospective Studies ,Superoxide Dismutase ,Glutathione ,Middle Aged ,medicine.disease ,Psychiatry and Mental health ,Oxidative Stress ,Endocrinology ,Logistic Models ,chemistry ,Female ,Lipid Peroxidation ,Oxidative stress - Abstract
Obsessive compulsive disorder is a common psychiatric disorder defined by the presence of obsessive thoughts and repetitive compulsive actions. The mutations or polymorphic variants in mitochondrial DNA-encoded genes or nuclear genes result in oxidative stress, which has recently been associated with various psychiatric disorders. In order to understand the association of mitochondrial disorders with oxidative stress in obsessive compulsive disorder, we examined genetic variants of manganese superoxide dismutase and uncouple-2 antioxidant genes and malondialdehyde and glutathione, markers of oxidative stress. The study sample comprised 104 patients with OCD and 110 healthy controls. For manganese superoxide dismutase, the frequencies of CT (Ala/Val) genotype (p < 0.01) in patients were significantly lower than those of controls. In contrast, CC (Ala/Ala) genotype was significantly more frequent in patients than controls (p < 0.05). For uncouple-2 I/D, the frequencies of ID genotype (p < 0.01) and I allele (p < 0.05) were lower in patients as compared with controls. In contrast, DD genotype was more prevalent in patients than controls (p < 0.01). While whole blood glutathione was significantly diminished (p < 0.0001), serum malondialdehyde was significantly elevated in patients compared with controls (p < 0.0001). Malondialdehyde levels were significantly elevated in subjects with DD genotype of UCP-2 I/D (p < 0.05) and CC genotype of manganese superoxide dismutase (p < 0.05) as compared with II or ID and TT or CT genotype, respectively. Malondialdehyde levels in patients carrying CC (p < 0.05) or CT (p < 0.05) genotype were significantly higher than those of carrying TT genotype. In conclusion, CC genotype of manganese superoxide dismutase or DD genotype of UCP-2 might result in mitochondrial disorders by increasing oxidative stress in obsessive compulsive disorders.
- Published
- 2011
15. The Effect Of Enalapril Maleat In Ischemia Reperfusion Injury: Possible Role of Membrane Bound Enzymes
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Makbule Aydin, Riza Dogan, Meltem Tuncer, and C. Selim Isbir
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chemistry.chemical_classification ,biology ,business.industry ,ATPase ,Ischemia ,Pharmacology ,medicine.disease ,Guinea pig ,Contractility ,Cell membrane ,Enzyme ,medicine.anatomical_structure ,chemistry ,Anesthesia ,biology.protein ,Medicine ,cardiovascular diseases ,Enalapril ,business ,Cardiology and Cardiovascular Medicine ,Reperfusion injury ,medicine.drug - Abstract
The present study evaluates the protective effect of enalapril maleat on myocardial ischemia-reperfusion injury. Membrane bound enzymes; Na(+)K(+)/Mg(2+) ATPase and Ca(2+)/Mg(2+) ATPase are known to regulate the membrane integrity. We hypothesized that if we could protect the cell membrane in ischemia-reperfusion period, we might have a chance to augment contractility. Thirty-two Guinea pig hearts were studied in an isolated Krebs-Henseleit solution-perfused Langendorff cardiac model. In Group 1, control hearts (n = 8) were arrested with St. Thomas Cardioplegic Solution (STHCS) alone. In Group 2 (n = 8), animals were pretreated with oral enalapril maleat (0.2mg/kg/daily) for ten days and arrested with STHCS. In Group 3, (n = 8) the hearts were arrested with enalapril maleat- (1 µmol/L) added STHCS. In Group 4 (n = 8), the hearts were again pretreated with oral enalapril maleat for ten days and then reperfused with enalapril maleat-added Krebs-Henseleit solution. Hearts were subjected to normothermic global ischemia for 90 minutes and then were reperfused at 37 degrees C. The study groups showed better recovery of left ventricular systolic function. In terms of biochemical determinations, best results were achieved at Group 4. The Na(+)K(+) ATPase and Ca(2+) ATPase levels were measured at 466.38 +/- 5.99 to 545.23 +/- 8.79, and 884.69 +/- 9.13 to 1254.34 +/- 1.56, respectively (p0.05). Based on these results, it can be concluded that enalapril maleat protects the membrane integrity and thus plays a role in restoring the contractility in ischemia-reperfusion injury./hea
- Published
- 2001
16. Ischemia/reperfusion in rat: antioxidative effects of enoant on EEG, oxidative stress and inflammation
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Sevilcan Tuna, Ilknur Özen, Makbule Aydin, Ihsan Kara, Asiye Nurten, Sacit Karamürsel, Bilge Özerman, and Elif Ozkok
- Subjects
Male ,medicine.medical_specialty ,Neurology ,Neuroscience (miscellaneous) ,Ischemia ,Inflammation ,Pharmacology ,medicine.disease_cause ,Antioxidants ,Brain Ischemia ,Beverages ,Basal (phylogenetics) ,chemistry.chemical_compound ,Random Allocation ,medicine.artery ,Developmental and Educational Psychology ,medicine ,TBARS ,Animals ,Vitis ,Common carotid artery ,Rats, Wistar ,business.industry ,Electroencephalography ,Glutathione ,medicine.disease ,Rats ,Oxidative Stress ,chemistry ,Anesthesia ,Reperfusion Injury ,Reperfusion ,Neurology (clinical) ,medicine.symptom ,business ,Oxidative stress - Abstract
The present study was undertaken to evaluate whether enoant, which is rich in polyphenols, has any effect on electroencephalogram (EEG), oxidative stress and inflammation in ischemia/reperfusion (I/R) injury.Ischemia was induced by 2-hour occlusion of bilateral common carotid artery. Animals orally received enoant. Group 1 was the ischemic control group. Group 2 was treated with enoant of 1.25 g kg⁻¹ per day for 15 days after I/R. Group 3 received the same concentration of enoant as in group 2 for 15 days before and after I/R. Group 4 was the sham operation group. EEG activities were recorded and the levels of TNF-α, IL-1β and IL-6, TBARS and GSH were measured in the whole brain homogenate.There were significant changes in EEG activity in groups treated with enoant either before or after ischemia when compared with their basal EEG values. TNF-α, IL-6 and IL-1β levels were significantly increased after I/R. GSH levels in group 3 treated with enoant in both pre- and post-ischemic periods were significantly increased and TBARS concentration was decreased compared with the ischemic group.The findings support that both pre-ischemic and post-ischemic administrations of enoant might produce neuroprotective action against cerebral ischemia.
- Published
- 2010
17. Angiotensin-converting enzyme polymorphism in schizophrenia, bipolar disorders, and their first-degree relatives
- Author
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Cem İsmail Küçükali, Elif Ozkok, Makbule Aydin, Ihsan Kara, Emine Bilge, Ulku Cakir, and Asli Zengin
- Subjects
Adult ,Male ,Future studies ,Bipolar Disorder ,Genotype ,Biology ,Peptidyl-Dipeptidase A ,Polymerase Chain Reaction ,law.invention ,law ,Genetics ,Humans ,In patient ,Family ,Genetic Predisposition to Disease ,Allele ,First-degree relatives ,Biological Psychiatry ,Genetics (clinical) ,Psychiatric genetics ,Polymerase chain reaction ,Alleles ,Polymorphism, Genetic ,Angiotensin-converting enzyme ,Middle Aged ,Psychiatry and Mental health ,biology.protein ,Schizophrenia ,Female - Abstract
Background Family, twin and adoption studies have provided major evidence for the role of genetics in numerous psychiatric disorders including schizophrenia (SZ) and bipolar disorders (BDs). As SZ and BD have some susceptibility genes in common and since unaffected first-degree relatives of these patients carry a high likelihood of these susceptibility genes, we aimed to elucidate the role of angiotensin-converting enzyme (ACE) genetic variants in patients with SZ, BD and their first-degree relatives. Methods The study sample comprised 239 patients with SZ, 184 patients with BD, 284 unaffected first-degree biological relatives of patients with SZ and 301 unaffected first-degree biological relatives of patients with BD and 210 healthy controls. The ACE genotypes were determined by polymerase chain reaction. Results ACE insertion/deletion polymorphism was associated with SZ and BD. DD genotype and D allele distributions in bipolar patients and their first-degree relatives were significantly higher than those of SZ patients, their relatives, and controls. In contrast, II genotype and I allele were reduced in both the patient groups and their relatives as compared with controls. Conclusion In this study, the D allele might be responsible for clustering of psychotic symptoms and results in the psychotic manifestations of BD, whereas I allele seems to be protective against development of SZ and BD. SZ and BD characterized by similar or different gene variant in ACE could be a useful marker for these psychiatric disorders, if this polymorphism is replicated in the future studies. Psychiatr Genet 20:14–19 � c 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins. Psychiatric Genetics 2010, 20:14–19
- Published
- 2009
18. Influences of genetic variants in interleukin-15 gene and serum interleukin-15 levels on coronary heart disease
- Author
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Makbule Aydin, Elif Ozkok, Ali Elitok, Cahide Gokkusu, Feti Tulubas, Berrin Umman, and Burak Pamukcu
- Subjects
Genotype ,Immunology ,Molecular Sequence Data ,Single-nucleotide polymorphism ,Coronary Disease ,Biology ,Biochemistry ,Polymorphism, Single Nucleotide ,Proinflammatory cytokine ,Polymorphism (computer science) ,Risk Factors ,Genetic variation ,Immunology and Allergy ,Humans ,Genetic Predisposition to Disease ,Molecular Biology ,Gene ,Aged ,Genetics ,Interleukin-15 ,Interleukin ,Hematology ,Middle Aged ,Restriction fragment length polymorphism - Abstract
Interleukin-15 (IL-15) is a potent proinflammatory cytokine that is now considered a key component of atherosclerosis. Proinflammatory gene polymorphisms lead to variations in the production and level of the proteins. In light of these findings, we hypothesized that variations in the gene coding for IL-15 influence the risk of coronary heart disease (CHD) by modulating the IL-15 levels. To test this hypothesis, we examined 5 single nucleotide polymorphisms (SNPs) in IL-15 gene and IL-15 levels in 102 patients with acute coronary syndrome (ACS), 102 patients with chronic ischemic stable CHD and 162 healthy control subjects. This study is the first report showing the influences of IL-15 gene variants and IL-15 levels on CHD. The five single nucleotide polymorphisms (SNPs) within the IL-15 gene, G367A, C267T, A14035T, C13687A, and A10504G were carried out by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum IL-15 levels were significantly higher in both acute and chronic patients than in controls. Genetic variants of IL-15 gene and IL-15 levels were associated with CHID. In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHID. Further studies are needed to confirm our hypothesis. (C) 2009 Elsevier Ltd. All rights reserved.
- Published
- 2009
19. Association Between Angiotensin-Converting Enzyme Gene Polymorphism and Coronary Artery Disease
- Author
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Bedia Agachan, Hulya Yilmaz, Makbule Aydin, Turgay Isbir, and C. Selim Isbir
- Subjects
Adult ,Male ,Candidate gene ,medicine.medical_specialty ,Turkey ,Clinical Biochemistry ,Coronary Disease ,Peptidyl-Dipeptidase A ,Biology ,Biochemistry ,Coronary artery disease ,Gene Frequency ,Risk Factors ,Internal medicine ,Genetics ,medicine ,Humans ,Myocardial infarction ,Allele ,Molecular Biology ,Alleles ,Aged ,Polymorphism, Genetic ,Angiotensin-converting enzyme ,Cell Biology ,Middle Aged ,medicine.disease ,Molecular biology ,Endocrinology ,Case-Control Studies ,Agarose gel electrophoresis ,biology.protein ,Female ,Gene polymorphism ,Restriction fragment length polymorphism - Abstract
An insertion/deletion (I/D) polymorphism in the gene for angiotensin-converting enzyme (ACE) is associated with myocardial infarction and other cardiac pathology. There is evidence for a role of the renin-angiotensin system in cell growth and in the repair of damaged arterial walls, so the ACE gene is postulated to be a candidate gene affecting the important clinical problem of coronary artery disease (CAD). In view of the clinical importance of the ACE as a major marker of cardiovascular diseases, we investigated the I/D polymorphism of the ACE gene in Turkish CAD patients in comparison with control subjects to evaluate a possible association between CAD and the gene encoding ACE. Polymerase chain reaction, restriction fragment length polymorphism, and agarose gel electrophoresis techniques were used to determine the ACE genotype in 58 subjects. The frequencies of ACE D and ACE I allele among the patients with CAD were 62.26% and 37.73 % and in the control subjects were 49.3% and 50.76%, respectively. The greater frequency of deletion allele (D) was in the CAD group than in the control subjects was significant (P < 0.01).
- Published
- 1999
20. Combined impact of matrix metalloproteinase-3 and paraoxonase 1 55/192 gene variants on coronary artery disease in Turkish patients
- Author
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Elif, Ozkök, Makbule, Aydin, Erhan, Babalik, Zeynep, Ozbek, Nurhan, Ince, and Ihsan, Kara
- Subjects
Adult ,Male ,Polymorphism, Genetic ,Genotype ,Turkey ,Aryldialkylphosphatase ,Myocardial Infarction ,Hyperlipidemias ,Coronary Artery Disease ,Middle Aged ,Hypertension ,Diabetes Mellitus ,Humans ,Female ,Genetic Predisposition to Disease ,Matrix Metalloproteinase 3 ,Alleles ,Polymorphism, Restriction Fragment Length ,Aged - Abstract
We investigated the association of matrix metalloproteinase-3 (MMP-3) and paraoxonase 1 (PON1) 55/192 polymorphisms with coronary artery disease (CAD) and the number of diseased vessels in patients with CAD.One hundred thirty-nine CAD patients and 119 healthy control subjects were included in the study. Genotypes for PON1 55/192 and MMP-3 5A/6A polymorphisms were determined by restriction fragment length polymorphism.Although distributions of the RR genotype of PON1 192 and the 5A5A genotype of MMP-3 were more frequent in patients, frequencies of the QQ genotype of PON1 192, the MM genotype of PON1 55, and the 6A6A genotype of MMP-3 were significantly lower in patients compared with healthy control subjects. The combined genotypes of RR/LL and/or 5A5A are increased the risk of CAD when compared with subjects who possess neither the MMP-3 5A5A nor the PON1 RR/LL genotype. While the MMP-3 5A/6A genetic variants were not associated with the number of diseased vessels, PON1 55/192 variants were associated with the number of diseased vessels.The combined PON1 55/192 and MMP-3 5A/6A genetic variants are associated with CAD; PON1 seems to be connected with the number of diseased vessels, and hypertension and hyperlipidemia are related with PON1 192 and MMP-3 in CAD patients.
- Published
- 2008
21. Association of genetic variants in Methylenetetrahydrofolate Reductase and Paraoxonase-1 genes with homocysteine, folate and vitamin B12 in coronary artery disease
- Author
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Feti Tulubas, Yesim Unlucerci, Elif Ozkok, Zeynep Ozbek, Burak Pamukcu, Berrin Umman, Makbule Aydin, and Cahide Gokkusu
- Subjects
Male ,medicine.medical_specialty ,Homocysteine ,Clinical Biochemistry ,Coronary Artery Disease ,chemistry.chemical_compound ,Folic Acid ,Internal medicine ,Genotype ,medicine ,Humans ,Vitamin B12 ,Cyanocobalamin ,Allele ,Molecular Biology ,Methylenetetrahydrofolate Reductase (NADPH2) ,Aged ,Genetics ,biology ,business.industry ,Aryldialkylphosphatase ,Paraoxonase ,Cell Biology ,General Medicine ,Middle Aged ,PON1 ,Vitamin B 12 ,Endocrinology ,chemistry ,Methylenetetrahydrofolate reductase ,biology.protein ,Female ,business - Abstract
Background The aim of the present study was to investigate the association between genetic variants in metylenetetrahydrofolate reductase (MTHFR) and Paraoxonase-1 (PON1) 55/192 genes and total homocysteine (tHcy), folate, B12 vitamin, and PON1 levels in patients with coronary artery disease (CAD). Methods The study included 235 patients with CAD and 268 healthy control subjects. Results LL and LM genotypes and L allele of PON1 55 were over-represented in patients. In contrast, MM genotype and M allele were more frequent in controls. QQ genotype and Q allele of PON1 192 and CT genotype of MTHFR were significantly diminished and QR genotype and R allele were significantly elevated in CAD patients compared with controls. The plasma tHcy were elevated but B12 levels were diminished in patients. PON1 55 and 192 genetic variants were significantly associated with PON1 activity, triglyceride, total cholesterol, tHcy and, high-density lipoprotein-cholesterol and low-density lipoprotein-cholesterol in patients, respectively. Conclusion Genetic variants of PON1 55/192 and MTHFR were associated with CAD.
- Published
- 2008
22. Effect of the methylenetetrahydrofolate reductase gene polymorphisms on homocysteine, folate and vitamin B12 in patients with bipolar disorder and relatives
- Author
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Ali Sazci, Elif Ozkok, Gamze Kilic, Zeynep Ozbek, Cem İsmail Küçükali, Nurcan Orhan, Makbule Aydin, and Ihsan Kara
- Subjects
Adult ,Male ,medicine.medical_specialty ,Bipolar Disorder ,Homocysteine ,Genotype ,chemistry.chemical_compound ,Folic Acid ,Gene Frequency ,Internal medicine ,Fluorescence Polarization Immunoassay ,medicine ,Humans ,Family ,Cyanocobalamin ,Vitamin B12 ,Bipolar disorder ,Allele frequency ,Biological Psychiatry ,Methylenetetrahydrofolate Reductase (NADPH2) ,Pharmacology ,Genetics ,Analysis of Variance ,Polymorphism, Genetic ,biology ,Homocystine ,Middle Aged ,medicine.disease ,B vitamins ,Vitamin B 12 ,Endocrinology ,chemistry ,Methylenetetrahydrofolate reductase ,biology.protein ,Female - Abstract
We investigated the effect of polymorphic variants of c.1298A>C (Glu429Ala) and c.677C>T (Ala222Val) in methylenetetrahydrofolate (MTHFR) gene on the total homocysteine (tHcy), folate and B12 levels in patients with bipolar disorder, first-degree relatives of patients, and controls. The c.677C>T and c.1298A>C polymorphisms in MTHFR were determined by polymerase chain reaction-restriction fragment length polymorphism in 197 bipolar patients, 278 relatives and 238 controls. tHcy and folate and vitamin B12 levels were measured by Fluorescence Polarization Immunoassay and Electrochemiluminescence, respectively. The tHcy was significantly increased in patients and relatives. In contrast, folate and B12 were significantly lower in patients and relatives. Gender was not considered as a significant determinant in the multivariate analysis. Genotypes of c.1298A>C and c.677C>T were correlated with tHcy, folate and B12. Patients and relatives carrying TT and/or AA and AC genotypes had elevated tHcy and reduced folate and B12 levels. High tHcy but low folate and vitamin B12 levels may be a risk factor for development of bipolar disorder.
- Published
- 2007
23. Are GRIK3 (T928G) gene variants in schizophrenia patients different from those in their first-degree relatives?
- Author
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Nurcan Orhan, Elif Ozkok, Gamze Kilic, Cem İsmail Küçükali, Asli Zengin, Makbule Aydin, and Ihsan Kara
- Subjects
Adult ,Male ,medicine.medical_specialty ,Psychosis ,Genotype ,Genetic determinism ,Gene Frequency ,Receptors, Kainic Acid ,Polymorphism (computer science) ,Internal medicine ,medicine ,Humans ,Family ,Genetic Predisposition to Disease ,First-degree relatives ,Allele frequency ,Biological Psychiatry ,Genetics ,Family Health ,business.industry ,Middle Aged ,medicine.disease ,Psychiatry and Mental health ,Schizophrenia ,Population study ,Regression Analysis ,Female ,business ,Polymorphism, Restriction Fragment Length - Abstract
We examined whether the GRIK3 (T928G) polymorphic variants in patients with schizophrenia are different from those of their first-degree relatives and healthy controls. The study population was composed of 256 patients with schizophrenia, 305 first-degree relatives of schizophrenia patients and 242 healthy control subjects. The GRIK3 (T928G) polymorphism was determined by restriction fragment length polymorphism. The frequency of the TT genotype was predominant, whereas the GG genotype was rare among all groups. The frequencies of GRIK3 (T928G) genotype distributions in the patients with schizophrenia were similar to those of their relatives. The frequency of the GG genotype was significantly higher in patients than in healthy controls. Similarly, GG genotype distribution in relatives was elevated compared with that in controls, but this value did not reach statistical significance. On the other hand, the subgroups of schizophrenia patients did not show a significant association with the GRIK3 (T928G) gene. It appears that the patients share the same (GRIK3) T928G gene variants with their relatives. One interpretation of our findings is that the relatives are at risk for the development of schizophrenia in the future.
- Published
- 2007
24. Relationship between interleukin-8 and the oxidant-antioxidant system in end-stage renal failure patients
- Author
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Makbule, Aydin, Elif, Ozkok, Oguz, Ozturk, Bedia, Agachan, Hulya, Yilmaz, Ilhan, Yaylim, Seher, Kebabcioglu, and Turgay, Ispir
- Subjects
Adult ,Male ,Malondialdehyde ,Interleukin-8 ,Humans ,Kidney Failure, Chronic ,Diabetic Nephropathies ,Enzyme-Linked Immunosorbent Assay ,Female ,Middle Aged ,Oxidants ,Glutathione ,Antioxidants - Abstract
We aimed to evaluate the relationship between interleukin-8 and the oxidant-antioxidant system in end-stage renal failure patients with and without diabetes mellitus undergoing regular hemodialysis treatment.Plasma levels of malondialdehyde and whole blood reduced glutathione were measured as markers of the oxidant and antioxidant systems, respectively. Plasma interleukin-8 levels were measured by enzyme-linked immunosorbent assay.When compared with controls, plasma interleukin-8 levels were elevated in both diabetic and nondiabetic end-stage renal disease patients. Plasma malondialdehyde levels were statistically significantly higher in end-stage renal disease patients with and without diabetes mellitus than they were in controls; however, reduced glutathione levels were statistically significantly lower in diabetic and nondiabetic end-stage renal disease patients than they were controls.In end-stage renal disease patients with and without diabetes mellitus, elevated interleukin- 8 levels and decreased reduced glutathione levels may be attributed to increased oxidative stress due to inflammation. In other words, increased reactive oxygen species may induce interleukin-8 production and result in diminished reduced glutathione levels. Our data suggest a relationship between interleukin- 8 and the oxidant-antioxidant system in end-stage renal failure patients.
- Published
- 2007
25. Is epsilon4 allele of apolipoprotein E associated with more severe end-organ damage in essential hypertension?
- Author
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Bedia Agachan, Turgay Isbir, Makbule Aydin, and Hulya Yilmaz
- Subjects
Apolipoprotein E ,Adult ,Male ,medicine.medical_specialty ,Heterozygote ,Apolipoprotein B ,Genotype ,End organ damage ,Clinical Biochemistry ,Blood Pressure ,Essential hypertension ,Left ventricular hypertrophy ,Biochemistry ,Polymerase Chain Reaction ,Retina ,Apolipoproteins E ,Gene Frequency ,Internal medicine ,medicine ,Humans ,Allele ,Alleles ,Polymorphism, Genetic ,biology ,Myocardium ,Homozygote ,Cell Biology ,General Medicine ,Middle Aged ,medicine.disease ,Endocrinology ,Hypertension ,biology.protein ,lipids (amino acids, peptides, and proteins) ,Female ,Hypertrophy, Left Ventricular ,Restriction fragment length polymorphism - Abstract
The aim of the present study comparing patients with mild to moderate hypertension with controls, was to explore a possible association between hypertension-related target organ damage and evaluation found in the gene encoding apolipoprotein E (apo E) genotype. Detailed medical history was recorded and physical examination was performed for all patients in the study (88 hypertensives, 63 normotensive controls). PCR (Polymerase Chain Reaction), RFLP (Restriction Fragment Length Polymorphism), and agarose gel electrophoresis techniques were used to determine the apo E genotypes. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 3.97, 88.06, and 9.95%, respectively in the hypertensive group. The frequencies of apo epsilon2, apo epsilon3, and apo epsilon4 alleles were 5.5, 92.0, and 2.38%, respectively in the control group. There were about twice as many individuals in the heterozygote hypertensive group who had apo E3/4 as compared to the control group (7.30 vs. 2.38%) (p = 0.07). The hypertensive patients who were carriers of the apo epsilon4 had significantly higher organ damage (left ventricular hypertrophy (p < 0.001). dilated left atrium (p < 0.05), retinopathy (p < 0.05)) as compared to those who were not carriers of apo epsilon4. These results showed a trend for the epsilon4 allele to be associated with a higher prevalence of target organ damage in patients with mild to moderate hypertension.
- Published
- 2001
26. Apolipoprotein-E gene polymorphism and lipid profiles in Alzheimer's disease
- Author
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Deniz Eker, Makbule Aydin, Ihsan Kara, Bedia Agachan, Turgay Isbir, Hulya Yilmaz, and Engin Eker
- Subjects
Apolipoprotein E ,Male ,medicine.medical_specialty ,Genotype ,Apolipoprotein E4 ,Biology ,Polymerase Chain Reaction ,Apolipoproteins E ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Polymorphism (computer science) ,Alzheimer Disease ,Internal medicine ,medicine ,Humans ,Allele ,Allele frequency ,Alleles ,Triglycerides ,Aged ,Genetics ,Aged, 80 and over ,Polymorphism, Genetic ,030214 geriatrics ,Cholesterol ,General Neuroscience ,Cholesterol, HDL ,Cholesterol, LDL ,Lipids ,Psychiatry and Mental health ,Clinical Psychology ,Endocrinology ,chemistry ,lipids (amino acids, peptides, and proteins) ,Female ,Gene polymorphism ,Geriatrics and Gerontology ,030217 neurology & neurosurgery - Abstract
In this study, the relationship between lipid profiles of sera and apolipoprotein E (apo E) gene polymorphism was investigated in 35 patients with Alzheimer's disease (AD) and 29 healthy people. Apo E genotypes and allele frequencies of the AD patient group were: apo E2/3, 2 (5.7 percent); apo E2/4, 1 (2.9 percent); apo E3/3, 26 (74.3 percent); apo E3/4, 5 (14.3 percent); apo E4/4, 1 (2.9 percent); epsilon 2, 3(4.2 percent); epsilon 3, 59 (84.2 percent); epsilon 4, 8 (11.4 percent). The healthy group's apo E genotypes and allele frequencies were: apo E2/3, 1 (3.4 percent); apo E3/3, 27 (93.1 percent); apo E3/4, 1 (3.4 percent); epsilon 2, 1 (1.7 percent); epsilon 3, 56 (96.5 percent); epsilon 4, 1 (1.7 percent). In Alzheimer's cases, epsilon 4 allele frequencies increased significantly as compared to the healthy group (p0.05). When the effects of the apo E isoforms on lipid profiles were evaluated, a relationship between apo E epsilon 4 allele and high total levels of serum cholesterol was found, whereas of apo E epsilon 2 allele was associated with the low total cholesterol of serum, although the difference was not statistically significant (p0.05). This study confirms the association of apo E epsilon 4 allele with lipid profiles in AD patients.
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- 2001
27. The protective effect of lisinopril on membrane-bound enzymes in myocardial preservation
- Author
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Bora Farsak, Riza Dogan, C. Selim Isbir, Makbule Aydin, and Kamer Kilinc
- Subjects
Time Factors ,Membrane bound ,ATPase ,Clinical Biochemistry ,Guinea Pigs ,Ischemia ,Myocardial Ischemia ,Angiotensin-Converting Enzyme Inhibitors ,Calcium-Transporting ATPases ,Pharmacology ,Sodium Chloride ,Biochemistry ,Thiobarbituric Acid Reactive Substances ,Potassium Chloride ,Guinea pig ,Calcium Chloride ,Lisinopril ,medicine ,Animals ,Magnesium ,Na+/K+-ATPase ,chemistry.chemical_classification ,biology ,Chemistry ,Myocardium ,Membrane Proteins ,Heart ,Cell Biology ,General Medicine ,medicine.disease ,Glutathione ,Perfusion ,Bicarbonates ,Oxidative Stress ,Enzyme ,Reperfusion Injury ,biology.protein ,Myocardial preservation ,Sodium-Potassium-Exchanging ATPase ,Reactive Oxygen Species ,circulatory and respiratory physiology ,medicine.drug - Abstract
A number of studies have reported that oxidant stress reduces the activity of isolated Na(+)-K(+) ATPase and Ca(2+) ATPase which are known to affect the cell membrane integrity. The aim of the study is to determine whether the administration of lisinopril is able to protect the membrane-bound enzyme levels in isolated guinea pig hearts and also ascertain whether or not a relationship exists between oxygen free radicals and membrane bound Na(+)-K(+) ATPase and Ca(2+) ATPase. Forty guinea pig hearts were studied in an isolated Krebs-Henseleit solution-perfused Langendorff cardiac model. In all groups cardioplegic arrest was achieved by administering St. Thomas' Hospital cardioplegic solution (STHCS). Group 1 (control, n=10) received only STHCS. Group 2 (n=10) were arrested with lisinopril (l micromol l(-1)) added STHCS. Group 3 (n=10) were pretreated with oral lisinopril (0.2 mg kg(-1) twice a day) for 10 days and then arrested with STHCS. Group 4 were also pretreated with oral lisinopril (0.2 mg kg(-1) twice a day for 10 days), arrested with STHCS and reperfused with lisinopril added to Krebs-Henseleit solution (l micromol l(-1)). Hearts were subjected to normothermic global ischaemia for 90 min and then reperfused at 37 degrees C. Pretreatment and addition of lisinopril in the reperfusion buffer improved the levels of membrane-bound enzymes. When the treated groups were compared with control hearts, the best results were achieved in group 4. The Na(+)-K(+) and Ca(2+) ATPase levels increased from 466.38+/-5.99 to 560.12+/-18.02 and 884.69+/-9.13 to 1287.71+/-13.01 nmolPi mg(-1) protein h(-1) respectively (p
- Published
- 2000
28. Age-related changes in GM1, GD1a, GT1b components of gangliosides in Wistar albino rats
- Author
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Hlya Yilmaz, Salih Cengiz, Turgay Isbir, Makbule Aydin, and Bedia A ahan
- Subjects
Brain Chemistry ,Male ,endocrine system ,medicine.medical_specialty ,Ganglioside ,Chemistry ,Clinical Biochemistry ,Age Factors ,Cell Biology ,General Medicine ,G(M1) Ganglioside ,Biochemistry ,Rats ,carbohydrates (lipids) ,Endocrinology ,Ageing ,Age related ,Internal medicine ,Gangliosides ,medicine ,Animals ,lipids (amino acids, peptides, and proteins) ,Rats, Wistar - Abstract
In this study, age-related changes of GM1, GD1a, GT1b fractions of gangliosides were investigated in whole brain of male Wistar albino rats. Insignificant increases were detected in GM1 values from the third to the 24th month, whereas GD1a and GT1b concentrations of ganglioside in 24-month-old rats decreased significantly as compared to 6-month-old rats. Although there were no significant differences in the GD1a/GT1b ratio of any groups, GM1/GD1a and GM1/GT1b ratios were significantly increased as compared to 6-month-old rats. The increase in the ratios of gangliosides are not due to an increase of GM1 fractions; they result from a decrease of GD1a and GT1b fractions of gangliosides. In conclusion, the concentration of ganglioside decreased with ageing.
- Published
- 2000
29. THE ROLE OF GLUTATHIONE PEROXIDASE 1 CODON 198 (GPX1 Pro198Leu) POLYMORPHISM IN PATIENTS WITH PROSTATE CANCER
- Author
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Canan Kucukgergin, Tzevat Tefik, Elif Ozkok, Makbule Aydin, Murat Gokpinar, Sule Seckin, Oner Sanli, and Ismet Nane
- Subjects
Prostate cancer ,GPX1 ,Polymorphism (computer science) ,business.industry ,Urology ,medicine ,Cancer research ,In patient ,medicine.disease ,business - Published
- 2008
30. Association of genetic variants in Methylenetetrahydrofolate Reductase and Paraoxonase-1 genes with homocysteine, folate and vitamin B12 in coronary artery disease.
- Author
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Makbule Aydin, Cahide Gokkusu, Elif Ozkok, Feti Tulubas, Yesim Unlucerci, Burak Pamukcu, Zeynep Ozbek, and Berrin Umman
- Abstract
Abstract Background The aim of the present study was to investigate the association between genetic variants in metylenetetrahydrofolate reductase (MTHFR) and Paraoxonase-1 (PON1) 55/192 genes and total homocysteine (tHcy), folate, B12 vitamin, and PON1 levels in patients with coronary artery disease (CAD). Methods The study included 235 patients with CAD and 268 healthy control subjects. Results LL and LM genotypes and L allele of PON1 55 were over-represented in patients. In contrast, MM genotype and M allele were more frequent in controls. QQ genotype and Q allele of PON1 192 and CT genotype of MTHFR were significantly diminished and QR genotype and R allele were significantly elevated in CAD patients compared with controls. The plasma tHcy were elevated but B12 levels were diminished in patients. PON1 55 and 192 genetic variants were significantly associated with PON1 activity, triglyceride, total cholesterol, tHcy and, high-density lipoprotein-cholesterol and low-density lipoprotein-cholesterol in patients, respectively. Conclusion Genetic variants of PON1 55/192 and MTHFR were associated with CAD. [ABSTRACT FROM AUTHOR]
- Published
- 2009
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31. Interaction between apolipoprotein-E and angiotensin-converting enzyme genotype in Alzheimer's disease
- Author
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Deniz Eker, Makbule Aydin, Ihsan Kara, Hulya Yilmaz, Engin Eker, Bedia Agachan, and Turgay Isbir
- Subjects
Apolipoprotein E ,Male ,medicine.medical_specialty ,Apolipoprotein B ,Genotype ,Peptidyl-Dipeptidase A ,Restriction fragment ,03 medical and health sciences ,0302 clinical medicine ,Apolipoproteins E ,Gene Frequency ,Alzheimer Disease ,Internal medicine ,medicine ,Humans ,Allele ,Allele frequency ,Aged ,Genetics ,030214 geriatrics ,biology ,business.industry ,General Neuroscience ,Angiotensin-converting enzyme ,Psychiatry and Mental health ,Clinical Psychology ,Endocrinology ,biology.protein ,Female ,Geriatrics and Gerontology ,Restriction fragment length polymorphism ,business ,030217 neurology & neurosurgery ,Gene Deletion ,Polymorphism, Restriction Fragment Length - Abstract
Both apolipoprotein-E (apo-E) epsilon 4 allele and angiotensin-converting enzyme (ACE) deletion (D) polymorphism have been associated with a high risk for coronary heart disease. Increased frequency of the epsilon 4 allele has also been reported in patients with late-onset of familial and sporadic Alzheimer's disease (AD). The primary aim of this study is to examine the possible relationship between the ACE gene polymorphism and AD. The second aim of this study is to explore the relation of the ACE and apo-E genotypes with AD. Polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP), and agarose gel electrophoresis techniques were used to determine the apo-E and ACE genotypes. The frequencies of ACE D and ACE insertion (I) allele among AD patients and controls were 55.7 percent versus 44.2 percent and 51.7 versus 48.2 percent, respectively. Apo-E allele frequencies in the AD group for epsilon 2, epsilon 3 and epsilon 4 were, 1.7 percent, 96.5 percent, and 1.7 percent, respectively. The apo-E allele frequencies of healthy groups for epsilon 2, epsilon 3 and epsilon 4 were 1 percent, 56 percent, and 1.7 percent, respectively. In conclusion ACE D and apo epsilon 4 allele were found to be more frequent in patients with Alzheimer's disease than in the control group.
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